The coronavirus that causes COVID-19, first identified in late 2019; it continues to evolve new variants and drive long-term health effects.
A team reporting in Nature grew human lung organoids whose own memory T cells, once boosted, blunt a later SARS-CoV-2 infection with no lymph node present. It gives a human in vitro way to study how much recall immunity to respiratory viruses the lung mounts locally.
Reality
Canadian researchers scanning 24 people with long COVID found fewer dopamine nerve endings in the striatum, a shortfall tied to a quarter of symptom variance. The result gives drug trials a dopamine hypothesis to test, though the scan reads a protein marker that stands in for the neurons themselves.
Reality
McMaster University researchers report that one flu or COVID infection sped motor decline in animal models of ALS. The work points to respiratory infection as an accelerant of the disease that treatment can blunt, but so far every result comes from animals.
Reality
Structural work on RE.2.2 from Gao George Fu's laboratory finds tighter receptor binding, a reshuffled antibody escape profile and a spike glycan at N529 that has not been seen in earlier SARS-CoV-2 variants.
Reality
An Institute for Systems Biology team names both the precursor cells and the signaling program behind them, which is what any drug program needs before it can start, though the published account reports no participant counts.
Reality
A Nature cohort of 1,154 hospitalized patients ties lingering anellovirus activity to physical disability, which puts the sampling schedule, not the cytokine panel, at the center of trial design.
Reality